The present invention relates to the field of ultrasound apparatuses and methods for non-invasive medical diagnostics and treatment.
In connection with performing medical diagnostics on the brain, it is often helpful to measure the variation, contraction or dilation, of blood vessels in the brain.
Currently known methods involve injection of radioactive or contrast-enhancing substances into the bloodstream in order to observe and learn about variations in blood flow in the brain between migraine attacks and normal conditions. Examination is also possible by the invasive method of introducing probes (electrodes) directly into the brain.
Currently known measurement methods for measuring blood flow to and in the brain include Isotope Diagnosis (ID) and Transcranial Doppler ultrasonography (TCD). Isotope Diagnosis is invasive and can only be performed by intermittent sampling measurements, rather that continuous measurement in real-time.
TCD is noninvasive and does give real-time measurement. However, the accuracy of the measurement is highly dependent upon the angle of the probe relative to the skull, and the skill of the operator. In addition, TCD does not measure the volumetric velocity of the blood flow and does not give precise measurement of the contraction or dilation of blood vessels in the brain. This imprecision is caused by the fact that TCD can only be used to observe a sector or large area in the brain, instead of a localized point. In addition, TCD uses ultrasound waves at a frequency of 2 MHz, which, for an estimated 15-40% of the population, do not actually reach the interior of the cranium, because of high attenuation of the ultrasound waves in the bone tissue of the cranium. In those cases, where there is a response from the skull or via xe2x80x9cacoustic windows,xe2x80x9d such as the temporal bones (orbital regions or foramen occipital magna), the acoustic reflections detected are only from the magistrial and proximal blood vessels. In addition to these reflected signals, this method also detects reflections from the brain and from other, non-cranial, blood vessels. The result is a noisy signal that does not allow precise determination of the depth of the measurement point. This does not allow measurement of individual blood vessels or their blood flow with any precision. Use of ultrasound technology as a diagnostic tool is discussed, inter alia, in the book entitled xe2x80x9cTextbook of Diagnostic Ultrasonography,xe2x80x9d 4.sup.th edition, by Mosby, pages 682-686.
It is also useful in connection with medical diagnostics of the brain to initially determine, and then monitor over time, the pressure in the brain. This pressure is commonly referred to in the art as intra-cranial pressure.
As a general rule, tissues in the body swell when traumatized. In order to heal, such tissues require oxygen. There are special circumstances with respect to brain tissue which makes the situation even more critical. The brain rests inside a bone casing, and there is little or no room for it to expand. When the brain swells, it experiences more trauma. Because it is encased within the skull, the swelling of the brain causes parts of the brain to be compressed. This compression decreases the blood flow and oxygen to parts of the brain which, in turn, causes more swelling. The more damage the brain receives, the more oxygen it needs, and the more it swells. Swelling is caused, e.g., by leakage from blood vessels. This leads to a rise in pressure within the brain. This rise in pressure rapidly equals the arterial pressure, thereby effecting the blood flow to the brain. The diffused pressure which decreases blood flow affects the ability of the cells within the brain to metabolize properly. The cells are unable to eliminate toxins, which toxins then accumulate in the brain. This phenomenon leads to a spiraling effect, which in effect is what kills brain-injured individuals who do not get prompt medical attention.
In response to a trauma, changes occur in the brain which require monitoring to prevent further damage. The size of the brain frequently increases after a severe head injury. This is referred to in the art as xe2x80x9cbrain swellingxe2x80x9d and occurs when there is an increase in the amount of blood in the brain. Thereafter, water may collect in the brain (referred to in the art as xe2x80x9cbrain edemaxe2x80x9d). Both brain swelling and brain edema result in excessive pressure in the brain. The pressure in the brain is referred to in the art as intracranial pressure (xe2x80x9cICPxe2x80x9d). It is essential that excessive ICP be identified and monitored so that it can be immediately treated. Treatment of brain swelling can be difficult, but it is very important because brain swelling in turn causes reduced amounts of both oxygen and glucose available to the brain tissue. Oxygen and glucose are both required by the brain to survive. The cranial cavity of the skull contains approximately 78% brain, 12% blood and vessels, and 10% cerebrospinal fluid (CSF). Intracranial volumes enclosed within the rigid container of the skull are fixed. An increase in the volume of one of these components requires an equivalent decrease in another of these components in order for the volume in pressure to remain constant. Increases in ICP occur as a result of this volume-pressure relationship. When there is an increase in any of these three components, the body tries to compensate by reabsorbing CSF and decrease intracellular volume.
In order to treat excessive ICP, physicians have a number of different methods available at their disposal, including the use of medications which help draw fluid out of the brain and into blood vessels; medications which decrease the metabolic requirements of the brain; medications which increase blood flow into the brain; and surgical procedures which are used to either reduce small amounts of fluid or remove the damaged brain tissue.
Surgical procedures further include removing any hematomas (blood clots) which are pressing on the brain, or surgically repairing damaged blood vessels to stop any further bleeding. In severe cases, portions of the brain that have been damaged beyond recovery may be removed in order to increase chances of recovery for the healthy portions of the brain. A shunt or ventricular drain may be used to drain off excess fluids. The overall goal of the neurosurgeon is to maintain blood flow and oxygen to all parts of the brain, thereby minimizing the damage and increasing the prospect of survival and recovery.
The normal values for intracranial pressure (ICP) at the level of foramen of Monro are approximately 90-210 mm of CSF in adults and 15-80 mm of CSF in infants. Increased ICP can occur as a result of an increased mass within the limited volume of the cranium. Examples include an increase in CSF volume, cerebral edema, and growing mass lesions such as tumors and hematomas. Cerebral edema is the increase in brain tissue water causing swelling. It may occur secondary to head injury, infarction or a response to adjacent hematoma or tumor. Uncorrected increased ICP can lead to further brain damage due to the pressure and inadequate blood perfusion of neurological tissues. The treatment for increased ICP includes removing the mass (tumor, hematoma) by surgery, draining CSF from the ventricles by a drain or a shunt, hyperventilation, steroids, osmotic dehydrating agents, and barbiturates.
Increased ICP will reduce cerebral blood flow, leading to ischemia. If blood flow is constricted for more than four minutes, an individual can experience irreversible brain damage. With constricted blood flow, cells become damaged, leading to more edema, causing more increased ICP.
The principle causes of elevated ICP include traumatic head injury (e.g., edema, intracranial hemorrhage, and hydrocephalus), infection, and tumors.
Treatment of elevated ICP can be accomplished by CSF drainage; decreasing the edema via the use of strong drugs such as diuretics; ventilation (mechanical and hyperventilation); cerebral perfusion pressure control (blood pressure control, fluid restriction); and promoting venous blood return; and intracranial surgery.
Most clinicians consider 20 mm Hg as the upper limited of acceptable ICP, beyond which treatment is initiated. The key to treatment is to control cerebral perfusion pressure (CPP) or the adequate flow of blood and oxygen to the brain cells. It has been shown that by monitoring ICP, treating brain edema and giving appropriate treatment, death and disability in humans can be decreased by more than 50%. Despite this positive outcome, monitoring of ICP was shown to be done in only 30% of patients with severe head injury, according to a survey of U.S. Trauma Centers.
The United States market for head injury is substantial with several unmet needs. In the United States, there are approximately two million cases of head injury per year. There are approximately 60,000 deaths per year due to head injury, with 500,000 hospital admissions per year and 20,000 in-hospital deaths per year due to head injury. Approximately 80,000 head injury survivors per year have a significant loss of function and require long-term medical and rehabilitation care. In fact, head injury is the leading cause of death and disability in ages 1-44. There are over 100,000 neurosurgical procedures done per year in the United States.
In the case of a head trauma, ICP can change significantly in a matter of minutes. Significant changes in ICP may also occur hours, days, or weeks, from diagnosis of the underlying trauma or disease state. It is therefore advantageous to continually monitor the ICP of a patient in an emergency room setting, in a surgical setting, and at a patient""s bedside.
Currently, the vast majority of ICP measurements are performed invasively, using needles, catheters, and implants.
In lumbar puncture, a needle is inserted at the base of the spinal column, to monitor the pressure of the fluid in the spinal column. This pressure may not reflect accurately the ICP, because there may be a blockage between the patient""s head and the base of the patient""s spinal column.
A second invasive method of monitoring ICP is to make a burr hole 5-10 mm in diameter in the patient""s skull and to introduce a catheter to one of the lateral ventricles via the hole. The pressure of the cerebrospinal fluid (CSF) in the ventricle is measured directly by a transducer via the catheter. This procedure may cause a hemorrhage that blocks the penetrated ventricle. In addition, if CSF enters the catheter, the accuracy of the pressure reading is impaired.
In a related invasive method, the catheter is held in place by a threaded fitting that is screwed into the patient""s skull. A saline solution is introduced to the catheter and the pressure of the saline solution is measured using an appropriate transducer. If insufficient care is taken to preserve antiseptic conditions, this procedure may lead to infection of the patient""s brain. Furthermore, the threaded fitting may penetrate the patient""s brain, causing damage to the patient""s brain.
In both of the latter two invasive methods, the catheter must be removed after five days. Therefore, these methods cannot be used for long term (several months) monitoring of ICP of patients in comas.
In a fourth invasive method, a fiber optic device, with a sensor at the tip of a fiber optic cable (available from Codman, a Johnson and Johnson Company), is inserted in the patient""s cerebral tissue, in the patient""s subdural space, or in the patient""s intraventricular and epidural space. If a blood clot forms on the sensor, or if the fiber optic cable bends too sharply or breaks, the device may give a spuriously high pressure reading.
In short, the prior art invasive methods of measuring ICP are unreliable, may lead to infection, and cannot be used for more than five consecutive days.
There are also additional drawbacks to invasive techniques. Due to the problems associated with invasive techniques for measuring ICP, standard medical protocol is to monitor ICP only for patients with scores of 8 or less on the Glascow Coma Scale. It would be useful to monitor ICP of patients with Glascow scores higher than 8. It would also be useful to monitor ICP in healthy individuals under severe environmental stress, such as astronauts, divers, and submariners.
A number of non-invasive techniques for measuring ICP have been proposed in the literature. However, for a variety of reasons, none of these methods have found significant commercial use.
For example, TCD has been used to provide a non-invasive, qualitative indication of variations in intra-cranial pressure (xe2x80x9cICPxe2x80x9d). The use of TCD in the measurement of ICP is described, for example, in Schoser B. G. et al., xe2x80x9cJournal of Neurosurgeryxe2x80x9d 1999, November: 91(5): 744-9; Nevell D. W., xe2x80x9cNew Horizonsxe2x80x9d 1995 August:3(3) 423-30, and PCT Publication WO 99/63890 to Taylor. Unfortunately, TCD only provides a qualitative indication of variations in ICP, and does not provide a quantitative measurement of ICP.
Attempts have been made to use TCD to obtain a quantitative measure of ICP using pulsatile (P.I.) and resistant (R.I.) indexes. However, according to the investigations done by Czosnika M. et al. xe2x80x9cJournal of Neurosurgeryxe2x80x9d, 1999, July 91(1) 11-9; and Hanlo P. W. et al. Child Neuro. Syst. 1995; October; 11(10); 595-603 there is no linear relations between ICP and TCD indexes. Moreover, the accuracy of these TCD measurements is low, particularly in patients with raised ICP.
Additional non-invasive methods for measuring ICP include xe2x80x9cclassical acoustic methodsxe2x80x9d based on the transfer of acoustic waves via the skull, as discussed in U.S. Pat. No. 5,117,835 to Edvin et al, and in O. Pranevicius et al, Acta Neurol. Sound 1992:86:512-516; and the Pulse Phased Locked Loop (PPLL) method as discussed in U.S. Pat. No. 4,984,567 to Kagaiama and in Uenot et al. xe2x80x9cActa Neurochir. Suppl.xe2x80x9d Wien 1998:71:66-9. These methods infer ICP by monitoring dura mater, a thick and dense inelastic fibrous membrane which lines the interior of the skull and extends inward to support and protect the brain.
However, classical acoustic and PLL methods are dependent upon the patients"" skull condition (e.g. skull fractures, skull thickness, and pneumocephalus) as well as the patient""s body temperature and environmental temperature. Each of these variables may lead to largely inaccurate ICP measurements. An additional disadvantage of these methods derives from their use of the thickness of dura mater as an indication of ICP despite the fact that dura mater, in some patients, may be adhered to the internal table of the skull. Moreover, the ICP waves generated by these methods do not resemble the ICP waves generated by invasive methods. This raises additional problems because doctors and nurses are not accustomed to reading and interpreting these types of ICP waveforms.
U.S. Pat. No. 5,617,873 to Yost et al, purports to describe an indirect, noninvasive method of monitoring ICP. Two changes in CSF volume are induced, and the associated changes in ICP are measured.
Therefore, presently known methods of quantitatively determining ICP remain predominantly invasive despite the existence of various non-invasive methods in the scientific and patent literature, and the need for a non-invasive alternative.
In addition to ICP, it is also useful in medical diagnostics to diagnose and monitor midline shift. The presence of midline shift provides an indication that some space filling lesion has caused distortion of the brain contents and, upon identification of the particular responsible mass, is normally cause for prompt intervention. Acute insults would be expected to initially induce elevation of ICP, with midline shift occurring later. Midline shift and ICP are thought to be closely related indicators of functional brain status following head trauma. However, it is generally believed that midline shift is a somewhat less sensitive indicator of acute unilateral space filling lesions than ICP. On the other hand, midline shift could well be a more sensitive predictor of slowly developing lesions such as brain tumors, where it serves as a confirmatory diagnostic tool, secondary to CT and MRI scans.
Under normal conditions, the brain sits in the middle of the cranial cavity equally distant from the outer limits of either hemisphere of the cavity. The brain is protected on all sides by cerebrospinal fluid.
A patient can experience edema, hemorrhaging/hematoma or some other lesion in the brain that will result in a shift away from midline, away from the hemisphere where the mass has formed. The key events that can cause such a shift are: traumatic head injury; post surgical hemorrhaging; infection; cerebrospinal fluid buildup; and/or the presence of a tumor. The shift may occur very quickly following the event or after a period of time.
Midline shift is currently measured by CT Scan. Determining midline shift is considered an important diagnostic tool by both neurosurgeons and emergency medicine physicians. A patient in the emergency room of a hospital presenting with a head injury and a low Glasgow Coma Scale score (8 or less), would be sent for a CT Scan. If the CT Scan is abnormal, showing a mass with or without midline shift, the neurosurgeon would be consulted. Sometimes the initial CT Scan is normal and the patient needs to be monitored. The question always arises as to what point does the patient get a second or third CT Scan. CT Scans are expensive, and the patient is subjected to radio-opaque dyes and contrast agents. Sending a seriously injured patient from the ER for a CT Scan can take the patient away from maximum emergency medicine care. The report on midline shift is typically fed back to the emergency medicine physician by the radiologist and presented qualitatively by categorizing the shift as minimal or substantial. In contrast, a neurosurgeon can read the CT Scan directly and determine the amount of shift (typically in millimeters).
Therefore, it would be advantageous to provide a portable, inexpensive technique to quantify midline shift which would be readily used in an emergency room or at a patient""s bedside.
In general, all of the prior art non-invasive methods described above derive ICP from data relating to only one of the structures in the intra-cranial space (e.g., brain tissue or ventricles or cisterns or vessels). TCD, for example, evaluates ICP only on the basis of certain properties of intra-cranial vascular system (P.I. and R.I.). This mono-causal approach makes TCD inherently inaccurate because it fails to take into account that ICP is a multi-causal parameter which is dependent on the characteristics of different areas of intra-cranial space and the different physiological relations between them. These factors include the brain""s tissue mass, the ventricular, cisternal and subarachnoid reserve space volume within the skull, the level of intra-cranial blood volume, and the input-output balance of intra-cranial blood flow.
Therefore, in order to provide an accurate, non-invasive measurement of ICP, it is important to take an integrated approach, which utilizes information regarding multiple contents and areas of intra-cranial space, and the mechanical and physiological relationship between them.
In view of the deficiencies in the prior art techniques discussed above, it is an object of the present invention to provide a non-invasive system for measurement of ICP which achieves some or all of the following criteria:
1. Provide a direct and real visualization of ICP waves in real-time which is visually similar to the ICP waves generated by current invasive methods, while providing long term registration and recording of ICP waves.
2. Provide high accuracy and resolution of measurement in real-time using an integrated approach which utilizes information regarding multiple contents and areas of intra-cranial space, and the mechanical and physiological relationship between them.
3. Provide accurate measurements that are not operator dependent and not dependent on the angle insonation of the ultrasound pulses.
4. Provide automatic real-time measurement of ICP.
5. Provide a device which can be operated by nurses without the assistance of a physician.
6. Provide a device which is cost effective.
The present invention is derived, in part, from the recognition that the soft tissue and fluid compartments of the brain each exhibit characteristic resonant responses to arterial pressure pulses that radiate through the tissues of the body. When a tissue of interest is stimulated by an ultrasound pulse, the nature of the reflected ultrasound signal will depend upon the resonant state of the tissue. Therefore, by properly processing and interpreting the reflected signal, it is possible to derive information relating to the physiological state of the tissue of interest.
In accordance with the present invention, an ultrasound probe is placed on the head of a patient, and is used to generate an ultrasound pulse which propagates through the skull and brain of the patient, and is reflected off of the skull and soft tissue lying in a path perpendicular to the ultrasound probe. The reflected signals are received by the ultrasound probe, and then processed in a known manner to generate an echo encephalogram (Echo EG) signal, which is plotted as a function of amplitude vs. distance. In this regard, the distance ordinate is obtained by converting the time delay from transmission of the ultrasound pulse to receipt of the reflected signals to the distance from the ultrasound probe to the point of reflection. A portion of the Echo EG signal is then selected, and the Echo EG signal is integrated over the selected portion to generate an echo pulsograph (EPG) signal. The selected position of the wave form corresponds to a selected distance from the ultrasound probe, and therefore corresponds to a discrete location in the brain which lies at a depth equal to the selected distance and in a path perpendicular to the probe. In accordance with one embodiment of the present invention, the selected portion has a width of 0.3 to 1.3 xcexcs, preferably a 0.3 to 1 xcexcs, and most preferably, a 0.5 to 0.7 xcexcs (corresponding to approximately one pixel and a depth of resolution of 0.5 mm). An electrocardiograph (ECG) signal for the patient is also generated in a known manner. Using the ECG signal as a reference, the EPG signal is used to provide information regarding the physiological state of the tissue at a depth from the ultrasound probe corresponding to the selected portion of the Echo EG signal.
Preferably, the ultrasound probe is placed either on the forehead of a patient, or on the back of the skull. When placed on the forehead, it is most preferably placed between 2 and 6 cm above the bridge of the nose when the desired point of interest is the third ventricle. In addition, the ultrasound pulse preferably has a pulse width between about 100 and 1000 ns, and a output intensity between about 50 and 300 mW/cm2. It should be noted that in the 95-98% of the world-wide population that have a frontal skull bone thickness of less than 2-3 cm, the output intensity can be lowered to, for example, 5 mW/cm2-10.5 mW/cm2, without adversely affecting the results thereby providing an output intensity range of between about 5 mW/cm2 and 300 mW/cm2 In that patient population, an output intensity range of from about 5 to about 10.5 or about 11 mW/cm2 should be sufficient.
In any event, it has been discovered that the pulse width and position described above, provides a substantially improved reflected signal as compared to the prior art methods described above. Within the above ranges, it should be noted that shorter pulse widths are generally preferable for investigating areas of the brain which are closer to the portion of the skull adjacent to the probe, and longer pulse widths are generally preferably for investigating areas of the brain which are further from the portion of the skull adjacent to the probe.
In addition, the ultrasound probe is preferably a probe having a concave shaped transmitting and receiving surface. As compared to a conventional ultrasound probe having a flat transmitting and receiving surface, the concave shaped probe in accordance with the present invention focuses the ultrasound signal on a significantly smaller area of brain tissue. For example, in accordance with the preferred embodiment of the present invention, the concave probe has cylindrical surface with a diameter of 28 mm a circular concave shaped transmitting and receiving surface extending to a depth of 1.3 mm. This probe will focus the ultrasound signal on an area of about 0.5xc3x971.5 mm (0.75 mm2) as compared with an area of 5 mm2 for a conventional flat probe of the same dimensions. Therefore, in the preferred embodiment described in more detail below, the concave shaped probe allows the system in accordance with the present invention to monitor an 0.5xc3x971.5xc3x970.5 mm portion of the brain. In accordance with one embodiment of the present invention, the EPG signal is used to provide a quantitative measure of intra cranial pressure (ICP) at a location of interest in the brain. In accordance with this embodiment, ICP is defined as follows:
ICP=xcfx81(t/T)*[t/T]xe2x88x92xcex2
wherein T is the time period between cardiac systoles, t is the time from the beginning of brain (e.g. cerebral) pulsatility to the peak following a venous notch (point xe2x80x9cBxe2x80x9d), xcex2 is a constant having a value of 9 mm H2O, and xcfx81(t/T) is a variable function greater than 0 and less than 1, which is characteristic of the particular brain tissue being monitored. For example, when measuring the ICP at the third ventricle of the brain, the central cerebral vein, and the lateral ventricle trigon or suprasellar cistern, xcfx81(t/T) is a substantially quadratic function, having a value of about 373 at t/T=0.3, a value of between 373 and 450 at t/T greater than 0.3 and  less than 1, and a value of less than 373 at t/T less than 0.2. Most preferably, xcfx81(t/T) has a value of about 325 at t/T=0.1, a value of between about 350 and 375 at t/T=0.2, and a value of less than 300 at t/T less than 0.05. In accordance with a further aspect of this embodiment, a frequency spectral and resonance analysis is performed on the EPG signal, and the second resonant frequency is used to more accurately identify the venous notch. Most preferably, the frequency spectral analysis is a discrete fourier transform.
In addition, the second resonant frequency is preferably used to further refine the calculated value for ICP. In this regard, for patients having a second resonant frequency of less than 4 Hz, ICP=xcfx81(t/T)*[t/T], and xcfx81(t/T) is a substantially quadratic function, having a value of about 150 at t/T= greater than 0.6, a value of between 100 and 150 at t/T greater than 0.1 and  less than 0.6, and a value of less than 100 at t/T less than 0.1.
For patients having a second resonant frequency of greater than 20 Hz, ICP=xcfx81(t/T)*[t/T]xe2x88x92xcex2, and xcfx81(t/T) is a substantially linear function for t/T greater than about 0.5, having a value of about 275 at t/T=0.5 and a value of about 675 at t/T=0.7.
In accordance with another embodiment of the present invention, the EPG signal is used to determine the width and position of ventricles and blood vessels. In accordance with this embodiment, opposing walls of a ventricle or blood vessel are identified by placing an ultrasound probe on an appropriate portion of the skull of a patient; transmitting an ultrasound pulse from the ultrasound probe into the skull of the patent; receiving a reflected signal from said ultrasound pulse; processing said reflected signal to generate a digital echo encephalogram signal; selecting a dominant portion of said echo encephalogram signal corresponding to the vessel or ventricle of interest; and integrating the echo encephalogram signal over the selected portion to generate an echo pulsogram signal, said echo pulsogram signal providing an indication of the pulsatility of a portion of the brain of the human patient corresponding to the selected portion of the echo encephalogram signal. The echo pulsogram signal is then identified as either a positive phase signal (i.e., a signal in which the maximum amplitude following a cardiac systole has a positive value) or a negative phase signal (i.e., a signal in which the maximum amplitude following a cardiac systole has a negative value). If the echo pulsogram signal has a positive phase, then the selected portion of the echo encephalogram is identified as corresponding the outer wall of the vessel or ventricle relative to the ultrasound probe. If the echo pulsogram signal has a negative phase, then the selected portion of the echo encephalogram is identified as corresponding the near wall of the vessel or ventricle relative to the ultrasound probe.
If a positive phase signal was identified, then a second portion of the echoencephalogram signal is selected which corresponds to a location in the brain which is closer to the ultrasound probe than the dominant portion selected previously. The echo encephalogram signal is then integrated over the selected second portion to generate an echo pulsogram signal. If the echo pulsogram signal is a negative phase signal, then the second portion of the echoencephalogram is identified as corresponding to the near wall of the vessel or ventricle. If the echo pulsogram signal is a positive phase signal, then successive second portions of the encephalogram are selected, which correspond to locations in the brain which are successively closer to the ultrasound probe, until a negative phase signal is identified.
If a negative phase signal was derived from the dominant portion of the echo encephalogram, then a second portion of the echoencephalogram signal is selected which corresponds to a location in the brain which is farther from the ultrasound probe than the dominant portion selected previously. The echo encephalogram signal is then integrated over the selected another portion to generate an echo pulsogram signal. If the echo pulsogram signal is a positive phase signal, then the second portion of the echoencephalogram is identified as corresponding to the far wall of the vessel or ventricle. If the echo pulsogram signal is a negative phase signal, then successive second portions of the encephalogram are selected, which correspond to locations in the brain which are successively farther from the ultrasound probe, until a positive phase signal is identified.
As set forth above, the echo encephalogram signal is a function of amplitude vs. distance from the probe to point of reflection of the ultrasound pulse. Therefore, the dominant portion of the echo encephalogram can be identified as corresponding to a first distance from the site of the probe, and the second portion of the echo encephalogram can be identified as corresponding to a second distance from the site of the probe. In this manner, both the position and width of the ventricle or vessel of interest are identified.
In accordance with a further embodiment of the present invention, the presence or absence of midline shift in a brain of a human patient is identified by: placing an ultrasound probe on a temporal area of a first side of the skull of a patient; transmitting an ultrasound pulse from the ultrasound probe into the first side temporal area of the patent; receiving a reflected signal from said ultrasound pulse; processing said reflected signal to generate a digital echo encephalogram signal; selecting a first-side dominant portion of said echo encephalogram signal corresponding to a third ventricle of the patient; integrating the echo encephalogram signal over the selected portion to generate a first-side echo pulsogram signal, said echo pulsogram signal providing an indication of the pulsatility of a portion of the brain of the human patient corresponding to the selected portion of the echo encephalogram signal. The first-side echo pulsogram signal, which corresponds to the first-side dominant portion, is then identified as a positive phase signal or a negative phase signal as described above.
Then, an ultrasound probe is placed on a second, opposite temporal area of a patient and an ultrasound pulse from the ultrasound probe is transmitted into the opposite temporal area of the patent. The reflected signal is then received and processed to generate a digital echo encephalogram signal, and a second-side dominant portion of said echo encephalogram signal is selected which corresponds to the third ventricle of the patient. The echo encephalogram signal is then integrated over the selected portion to generate an second-side echo pulsogram signal. The second-side echo pulsogram signal, which corresponds to the second-side dominant portion, is then identified as a positive phase signal or a negative phase signal as described above. If the first and second side echo pulsograms have the same phase, then they are identified as corresponding to opposing walls of the third ventricle. The first-side dominant portion of the echo encephalogram can be identified as corresponding to a first distance from the first side temporal area, and the second-side dominant portion of the echo encephalogram can be identified as corresponding to a second distance from the second side temporal area. Based on the assumption that the third ventrical is substantially symetrical, and normally centered on the midline of the brain, the first distance should equal the second distance for a patient with no midline-shift. The midline shift in a patient can therefore be quantified as (first distancexe2x88x92second distance)÷2.
Preferably, the method also includes identifying the position of the opposing ventrical wall by locating the opposite phase signal (i.e. a positive phase signal if the dominant portion generated a negative phase signal, and vice versa) in the manner described above with regard to the method of identifying the width and position of a vessel or ventricle wall.